Chapter 14. Biology and Diseases of Ferrets Flashcards
Ferret taxonomy
Family Mustelidae
Subfamily Mustelinae
Genus Mustela
Mustela putorius furo
Subfamily Mustelinae
Includes weasels, mink, ferrets (genus Mustela), martens (genus Martes)
Genus Mustela
5 subgenera: Mustela (weasels), Lutreola (European mink), Vison (American mink), Putorius (ferrets) Grammogale (South American weasels)
Family Mustelidae
- Smallest member = least weasel (Mustela nivalis)
- Largest member = sea otter (Enhydra lutris)
Ferret use in research
- Influenza pathogenesis
- Virology
- Neuroscience
- Carcinogenesis
- Cardiovascular physiology
- Emesis
Sources of ferrets
- Large-scale commercial production (available in US) - inbreeding related to disease susceptibility?
- Fur operations
Commercials stocks of ferrets
-Based on coat color: albino, sable (‘fitch’, ‘wild’; most common), Siamese, silver mitt, Siamese-silver mitt (Siamese with white chest and feet)
US ferrets with blaze or white head
- Up to 75% can have Waardenburg syndrome & are deaf
- Physiologic basis: ipsilateral projections of the cochlear nucleus to the auditory midbrain in albino ferrets
- Albino ferrets also have impaired motion perception & contrast sensitivity
Recommended temperature ranges for ferrets
- Tolerate low temps well & high temps poorly
- Juveniles & adults: 4-18 C (39.2-64.4 F)
- <6 weeks old: greater than 15 C; kits under this age require a heat source if separated from dam; older group-housed kits do not
- Elevated temps (>30 C; 86 F) cannot be tolerated by ferrets
Why can’t ferrets tolerate high temperatures?
Poorly developed sweat glands = susceptible to heat prostration
-Signs of heat stroke: panting, flaccidity, vomiting
Recommended humidity range for ferrets
40-65%
Recommended lighting for ferrets
- 12:12 dark-light appropriate for non-breeding animals housed for <6 months
- 16 hr light daily for breeding and lactating jills
- Ferrets maintained beyond 6 mths should be exposed to a ‘winter’ = 6 weeks per year of 14 hr dark daily to maintain physiologic normalcy
Light cycle for time-pregnant jills
Maintain light cycle that time-pregnant jills were exposed to prior to shipment; failure to do so can results in negative energy balance & pregnancy toxemia
Recommended air changes for ferret housing
- 10-15 air changes per hour
- Use nonrecirculated air b/c of strong ferret odor & susceptibility of ferrets to human respiratory tract infections
- Ferret odor should not overlap any rodent housing areas b/c rodents have instinctive fear of ferrets; scent can disrupt rodent breeding and physiology
Social housing of ferrets
- Females can be housed singly or in groups
- Estrous females that are cohoused may become pseudopregnant
- Intact males should be housed individually after 12 weeks of age
- Weanling ferrets (4- 12 week old) may be group housed
Spacing of grid wall for ferret caging
1 x 0.5 inches apart, or 0.25 inch if using wire mesh
Potentional health concerns for ferret caging
- Zinc toxicosis reported in ferrets licking galvanized bars from which metals had leached during steam sterilization
- Clay litters can cause chronic upper resp infx due to inhaled dust
Cage size for ferrets
24x24x18 inches = adequate for 2 adults
Diet parameters for ferrets
- Protein source: meat
- Nonbreeding adults = 18-20% fat, 30-40% protein
- Breeding adults = 25% fat, minimum 35% protein
- Peak lactation = minimum 30% fat, minimum 35% protein
Food and water consumption of ferrets
- Feed ad libitum
- Food: 43 g/kg body weight
- Water: 75-100 mL daily
Enrichment for ferrets
- Sleeping locations: snooze tube, hammock, PCV pipe or dryer hose
- Digging behavior: box filled with rice, plastic balls, crumpled paper balls
- Enrichment lowers fecal glucocorticoid metabolites (FGM) in juvenile males; this study also showed juvenile males interacted with enrichment more than juvenile females (no effect on juvenile female FGM)
Unique anatomy of ferrets - thorax
- Thorax is narrow & elongated with proportionally long trachea = good for studies of tracheal physiology
- Tracheal size & laryngeal anatomy make intubation somewhat challenging = ferrets used for pediatric intubation training
- Lung relatively large; total lung capacity is nearly 3x what would be predicted based on body size compared to other mammals = pulmonary research model
- Higher degree of bronciolar branching with more extensive bronchial submucosal gland compared to dog = pulmonary research model
- Paired common carotid arteries arise from the brachiocephalic trunk at the level of the thoracic inlet (like dogs & cats)
Unique anatomy/physiology of ferrets - abdomen
- Carnivore = simple monogastric stomach
- NO cecum; indistinct ileocecal transition makes it difficult to identify junction of small and large intestines grossly
- Length of alimentary tract is very short relative to body size = GI transit time as short as 3 hr
- Extramedullary hematopoiesis common in spleen; can result in splenomegaly
- Ferrets have no naturally occurring antibodies against unmatched erythrocyte antigens & none develop even with repeated transfusions
Scent glands of ferrets
- Paired anal scent glands; well-developed
- Animals can be descented surgically
- Some animals, especially intact males & estrous jills, may still have musky odor even after descenting because of normal sebaceous secretions
Sweat glands of ferrets
-Ferrets lack well-developed sweat glands = predisposed to prostration when ambient temps reach 32 C (90 F)
Unique anatomy/physiology of ferrets - reproductive
- Seasonal breeders
- Prolonged estrus in unbred females can result in aplastic anemia - can reproduce this with exogenous estrogen administration
- Males has os penis & prostate gland
Ferret weight ranges
- Newborn kits: 6-12 g at birth
- 6-8 weeks: 400 g
- Intact males: 1-2 kg
- Intact females: 0.5-1 kg
- Gonadectomized adults: 0.8-1.2 kg
- Body weight can fluctuate up to 30-40% with seasonal changes
Ferret lifespan
6-8 years; rarely up to 11 years
Normal body temperature for ferrets
38.8 C (37.8-40 C)
Chromosome number for ferrets
40 (diploid)
Dental formula for ferrets
2 (I 3/3, C 1/1, P 4/3, M 1/2)
Vertebral formula for ferrets
C7-T15-L5-S3-C14
Age of sexual maturity for ferrets
4-12 months
-Length of breeding life is 2-5 years
Gestation length in ferrets
42 +/- 2 days
-Litter size 1-18, average 8
Kit development in ferrets
- Birth weight: 6-12 g
- Eyes open: 34 days
- Onset of hearing: 32 days
- Weaning: 6-8 weeks
Erythron in ferrets
-Ferrets have relatively robust erythron, with Hct, Hbg, and total RBC & reticulocyte counts generally higher than dog or cat
Proteinuria in ferrets
- A low grade proteinuria on UA may be seen in normal, healthy ferrets
- Normal USG in intact males: 1.051, intact females: 1.042
Ferret nutrition
- Strict carnivores
- Short GI tract & rapid GI transit time require protein to be readily digestible
- Daily maintenance energy requirement: 0.5 MJ metabolizable energy (ME)/kg metabolic body weight (BW^0.75)
- In MINK: 42% protein up to 16 weeks; after 16 weeks old, 26-36% protein, 9-28% fat, 22-42% carbohydrate
- 30-40% protein & 18-20% fat for adults; minimum 35% protein & 25% fat for reproductively active & growing animals
- Diets high in fish or with raw meat not recommended
- Digestibility of crude protein in ferrets significantly lower than cats & digestibility of crude fat significantly higher = ferrets cannot be used as a model of cats & careful comparing data between two species
- Carbohydrates should not exceed 30-36% for adults, but kits feed carb-free diet reported to do poorly d/t hypoglycemia
High levels of plant protein in ferret diets
Can lead to urolithiasis
Ferrets in Beta-carotene research
- Used to investigate absorption, metabolism, interaction of Beta-carotene & Vit E
- Ferrets, like humans, convert Beta-carotene to Vit A in the gut & absorb Beta-carotene intact
- Beta-carotene, retinol & retinyl esters are absorbed intact into the lymph & cleavage products (Beta-apo-12’-carotenal, Beta-apo-10’-carotenal, retinoids) accumulate in intestinal mucosa - mucosa converts Beta-carotene into retinoic acid - transported via portal vein to liver
- Beta-carotene absorption & conversion into retinol enhanced by coperfusion of alpha-tocopherol
- Ferrets able to excrete retinol & retinyl esters into urine - depends on oral Vit A supplementaton
- Lung cancer model of ferrets exposed to tobacco smoke has been used to evaluate the cancer-modulating properties of these micronutrients
Ferret water consumption
- 75-100 mL per day, depending on dry matter content of feed
- Provide fresh water ad libitum in secured bowels or water bottles (ferrets will overturn is not well secured)
Ferret reproductive calendar
- Seasonal breeders
- In the wild, season in Northern Hemisphere is March-August for females & December-July for males
Estrous cycle in ferrets
- -Puberty: 6-12 months
- Minimum breeding age: 8-12 mths male, 4-5 mths female
- Monestrous, continuous duration until intromission
- Induced ovulators
- Jills maintained at 8 hr light-16 hr dark reach puberty in 10-12 months
- The transfer from short to long photoperiods should not occur prior to 90 days of age, b/c jills that are prematurely transferred will remain anestrous
Gestation period in ferrets
42 +/- 1 day
-Average litter size 8 (1-18)
Estrus in ferrets
- Vulvar swelling is hallmark sign
- NOT assoc w/ rising FSH like in rodents
- Mated ~14 days after vulvar enlargement
- Estradiol concentrations responsible for development of female reproductive tract & secondary sexual characteristics
- Tonic inhibition of LH secretion by the anterior pituitary during both prepubertal life and anestrus
- With increasing light exposure, LH levels rise despite estradiol
- Jills may return to estrus during 2nd-3rd week of lactation if they have fewer than 5 kits, or 2 weeks after weaning if litter is larger
- Jills should be rebred or given hCG to terminate estrus, even if still lactating
- May have 2-3 litters yearly until 5 years old
- A nonstimulatory photoperiod should be used 6 weeks per year to rest the ferret and preserve maximum fertility - jills return to estrus ~3 wks after reinstitution of longer photoperiod
- Return of estrus correlates with follicular development and increased plasma estradiol
Reproductive physiology of male ferrets
-Age differences in the sensitivity of negative feedback inhibition of the hypothalamic secretion of gonadotropin-releasting hormone (GnRH) by testosterone, or to estrogenic compounds derived from aromatization of testosterone, appear to be essential in determining puberty & seasonality of reproduction in males
Ovulation in ferrets
5-13 ova ovulated 30-40 hr after coitus = induced ovulators
- Neck restraint and intromission by the male required for ovulation
- Implantation occurs 12 days after mating
Placentation of ferrets
-Zonary & endotheliochorial (typical for carnivores)
Pregnancy detection in ferrets
- Ultrasound detection as early as day 12
- Palpation as early as day 14
- Calcified fetal skeletons on radiographs at ~30 days
Husbandry needs of pregnancy ferrets
- Separate to single housing when within 2 weeks of parturition
- Provide nest box with bedding for warmth
- Next box should be at least 6 inches deep
- Nutritional support very important: risk for pregnancy toxemia = hypoglycemia, hyperketonemia, hypoinsulinemia, decreased T4 & T3, hepatic lipidosis
Parturition in ferrets
- Rapid, as little as 2-3 hr
- Primiparous jills usually deliver on day 41, multiparous on day 42
- Fetuses remaining in utero beyond day 43 typically die
- Dystocia is common d/t positional abnormalities and fetal oversize = C-section; failure to deliver within 8 hr after administration of prostaglandin is indication for C-section
- Leave undisturbed for several days postpartum to minimize cannibalization
- Fostering: allow pups to mingle with foster jill’s own pups while jill is away so that rejection d/t olfactory stimuli will not occur
Development of newborn ferrets
- Born altricial; dependent on jill for first 3 weeks
- Coat color starts to become visible at 3 days of age
- Weigh 6-12 g at birth
- Sexual dimorphism in size apparent by week 7
- Eruption of deciduous teeth = 14 days
- Ability to hear = 32 days - ear canals do not open until 32 days - startle response in kits
- Opening of eyes = 34 days
- Eruption of permanent canines = 47-52 days
- Displacement of deciduous canines by 56-70 days
- POLECATS = learn scent of prey between 60-90 days
Weaning in ferrets
- 6 weeks of age
- Can give slurry of adult food with fat supplementation to achieve 30% fat (Linatone supplement)
- Diet should be 30% fat, 40% protein
- Group housed until sexually mature
- Males >12 weeks old may fight if exposed to greater than 12 hr of light per day
Clostridium perfringens Type A - etiology, transmission
- Etiology: Clostridium perfringens Type A
- Ubiquitous, present in GI tracts of humans & animals
- Acute abdominal distenstion, dyspnea, cyanosis in weanling ferrets
- Predisposing factors: overeating, sudden changes in diet, proliferation of C. perfringens type A & its toxins
Toxins of Clostridium perfringens Type A
-Alpha toxin: principal lethal toxin; hemolytic and necrotizing & has ability to split lecithin or lecithin-protein complexes, leading to destruction of cell membranes & necrosis
Clostridium perfringens Type A - clin signs, diagnosis
- Clin signs: acute abdominal distension, cyanosis, found dead & bloated
- Diagnosis: isolation of bacteria from stomach/intestines; toxin identification using mouse protection assay
- Necropsy findings: markedly distended stomach & intestines with large amount of gas & brown semiliquid ingesta; SC emphysema
- Histo: abundant G(+) bacilli in smears of gastric and intestinal contents; GI mucosa necrosis, G(+) baclli lining denuded mucosal surface & extending into gastric glands, intestinal crypts; lymphoid necrosis of LNs, spleen, thymus; mild to moderate dilation of central hepatic sinusoids with hepatocellular dissociation and multifocal aggregates of necrotic neutrophils within portal areas
Clostridium perfringens Type A - treatment, control
- Prevention: good management & feeding practices; restrict feeding of weanlings to 2x instead of 3x daily
- Tx: supportive care, gastric trocharization - these can be unrewarding
Campylobacteriosis - etiology, transmission
- Etiology: Campylobacter jejuni; G(-) spirally curved microaerophilic bacteria
- Causes diarrheic illness in humans, dogs, cats, cows, goats, pigs, mink, ferrets, sheep; mastitis in cows, infectious hepatitis in chickens; abortion in cattle, sheep, goats, dogs, mink
- Can be cultured from asymptomatic dogs, cats, ferrets
- Transmission: ingestion of organisms through direct contact with feces or contaminated feed & water
Campylobacteriosis - clin signs, diagnosis
- Clin signs: self limiting diarrhea; anorexia, dehydration, tenesmus; fetal resorption, abortion
- Diagnosis: based on history, clinical signs, culture - grows slowly & need selective media or filtration techniques w/ temp 42-43 C & microaerophilic conditions; round, raised, translucent & sometimes mucoid colonies
- Ddx: proliferative bowel disease, other infectious and noninfectious causes of diarrhea
Campybacteriosis - pathology, treatment, control
- Necropsy findings: neutrophilic infiltrates in lamina propria of colon; enterocolitis; placentitis
- Tx: supportive care, antibiotics based on C&S; azithromycin & fluoroquinolones commonly used in humans; experimental killed whole cell vaccine protected 80% of ferrets when given 4 doses 48 hr apart
- Control: ZOONOTIC = isolate positive animals; good hygiene
Helicobacter mustelae - etiology, transmission
- Isolated from margins of a duodenal ulcer of a ferret
- Every ferret with chronic gastritis is infected with H. mustelae; SPF ferrets do not have gastritis, gastric ulcers, or detctable IgG antibody
- Robust model for H. pylori gastritis in humans
- Colonizes nearly 100% of ferrets shortly after weaning; may be due to fecal-oral transmission
- Ferrets placed on proton pump inhibitors, which raise gastric pH, have a statistically higher recovery of H. mustelae from feces when compared with age-matched untreated control ferrets
- Ferret is ONLY domesticated animal to date with naturally occurring helicobacter associated ulcer disease
Helicobacter mustelae - clin signs, diagnosis
- Clin signs: gastric or duodenal ulcers - vomiting, melena, chronic weight loss, lowered hematocrit; gastric adenocarcinoma - vomiting, anorexia, weight loss
- Ddx: gastric foreign body
- Dx: endoscopy; gastric samples inoculated onto blood agar plates supplemented with trimethoprim, vancomycin, polymixin B - incubate at 37 or 42 C in a microaerobic atmosphere for 3-7 days; H. mustelae = produce urease, catalase, oxidase; resistant to cephalothin; sensitive to nalidixic acid
Helicobacter mustelae - pathology, treatment, control
- Superficial gastritis with H. mustelae on surface of mucosa but NOT in crypts; diffuse antral gastritis; focal glandalar atrophy (a precancerous lesion) & regeneration; can see deep colonization focally in antrum
- Argyrophilic bacteria in liver, biliary tract - chronic cholangiohepatitis, bile duct hyperplasia, cholangiocellular carcinoma (H. cholecystus)
- Susceptible to gastric cancer = gastric adenocarcinoma, gastric mucosa associated lymphoid tissue (MALT) lymphoma
Helicbacter mustelae - treatment, control
- Tx: triple therapy with amoxicillin, metronidazol, bismuth subsalicylate 3x daily for 3-4 weeks; ranitidine bismuth & clarithromycin 3x daily for 2 weeks
- Eradicaton associated with decrease in anti-H. mustelae IgG antibody titers (consistent with findings in humans)
- Omeprazole induces hypochlorhydria & may be used in conjunction with antibiotics to treat H. mustelae-assoc duoenal or gastric ulcers; cimetidine can also be used to decrease acid secretion; sucralfate for clinical signs of stomach ulcers
- Fluids & blood transfusions for acute bleeding ulcers
Proliferative bowel disease in ferrets - etiology, transmission
- Etiology: Lawsonia intracellularis = intracellular Campylobacter-like organisms related to Desulfovibrio spp.; G(-), comma to spiral-shaped bacteria
- Transmission: fecal-oral
- Disease of young ferrets
- Copathogens include Campylobacter spp, coccidia, chlamydia
Proliferative bowel disease - clin signs, diagnosis
- Clin signs: chronic diarrhea, lethargy, anorexia, weight loss, dehydration; diarrhea may be blood-tinged, contain mucus, often green in color; rectal prolapse; ataxia and muscle tremors
- Dx: clinical signs, palpably thickened colon, colonic biopsy
- Ddx: other causes of diarrhea and weight loss
Proliferative bowel disease - pathology, differentials, treatment
- Segmented, thickened large bowel - usually terminal colon, can also include ileum and rectum
- Histo: marked mucosal proliferation and intracytoplasmic L. intracellularis seen with silver stain in apical portion of epithelial cells; mixed inflammatory infiltrate; reduced goblet cell production; hyperplasia of glandular epithelium; glandular irregularity with penetration of mucosal glands through the muscularis mucosa; increased thickness of tunica muscularis
- Translocation of glandular tissue to extraintestinal sites - regional LNs & liver - has been reported
- Ddx: other causes of diarrhea and wasting, including dietary changes, eosinophilic gastroenteritis, gastric foreign body, lymphoma, Aleutian disease (AD), gastric ulcers
- Incidence appears to be rare
- Tx: supportive care; chloramphenicol or metronidazole for 2 weeks
Tuberculosis in ferrets - etiology, transmission
- Etiology: Mycobacterium bovis, M. avium, M. tuberculosis
- Aerobic, G(+), non-branching, non-spore-forming, acid-fast rods
- Ferrets might be more susceptible to mycobacterial infections than other species; can have natural infections with M. bovis and M. avium; also susceptible to experimental infx with human tubercle bacillus; endemic in feral ferrets inf New Zealand
- Feeding of commercial diets and TB testing in livestock and poultry has reduced incidence of the disease in ferrets
- Horizontal transmission demonstrated in ferrets under experimental housing conditions
- Den sharing, playing, fighting, sniffing, cannibalism, and aggressive breeding could transmit TB between ferrets
- M. celatum infx reported in one ferret - accurate dx difficult because reacts positively with polyclonal Abs against M. paratuberculosis & M. bovis = identify using 16S rRNA sequence analysis
Tuberculosis in ferrets - clin signs, pathology
- M. bovis causes typical microscopic foci of infection & necrosis; M. avium may not cause these in all ferrets; human TB causes just localized infx with minor spread to adjacent LNs
- Weight loss, anorexia, lethargy, death, miliary lesions of lungs & other viscera, progressive paralysis
- Mesenteric LNs often infected - related to ORAL infection
- Histo: granulomatous inflamm w/ predominantly macrophages, multnucleated giant cells, epithelioid cells - in lungs, intestines, spleen, liver, peripancreatic adipose tissu; numerous acid-fast bacilli within macrophages
- Impaired cell-mediated response may account for the large number of organisms observed in M. bovis lesions
Tuberculosis in ferrets - diagnosis, treatment, control
- Dx: isolation of organism in tissue; most common sites = retropharyngeal & mesenteric LNs
- A tuberculin skin testing regimen has NOT been definitively characterized for ferrets yet
- Tx: euthanasia b/c ZOONOTIC; clarithromycin, rifampicin, clofazimine
Salmonellosis in ferrets - etiology, transmission
- G(-), non spore forming, facultative anaerobic rods in family Enterobacteriaceae
- Genus Salmonella has 2 species: S. bongori = poikilotherms & rarely humans, S. enterica
- Transmission: ingestion from contaminated food or water products
- Serotypes that have been isolated from ferrets include S. Hadar, S. Enteritidis, S. Kentucky, S. Typhimurium
Salmonellosis in ferrets - clin signs, pathology
- Conjunctivitis, rapid weight loss, tarry stools, febrile, lethargy, anorexia, trembling, abortion/stillbirth
- Gross lesions: tissue pallor, petechiae of gastric mucosa, melena, dark fibrinous exudate in large intestine, GI contents containing lots of mucus, some blood
- Histo: desquamated epithelium of GI mucosa, exudate in small intestine containing mucoid material, RBCs, desquamated intestinal villi; edematous villi in ileum, infiltration of small intestinal mucosa with lymphocytes and macrophages; necrotic foci in liver, spleen, kidney; splenomegaly, visceral lymphadenopathy; necrotizing endometritis
Salmonellosis in ferrets - diagnosis, treatment, control
- Dx: based on history, clinical signs, isolation of organism - culture on enrichment and selective media
- Tx: sulfathalidine in feed; supportive care; antibiotics based on C&S
Pneumonia in ferrets
- Streptococcus zooepidemicus & other group C & G streptococci; Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, Bordetella bronchiseptica
- Primary bacterial pneumonia not very common; may occur secondary to megaesophagus in ferrets, or secondary to influenza
- EXCEPTION: outbreak of Mycoplasma species in ferrets as primary pathogen
- Clin signs: nasal discharge, dyspnea, lethargy, anorexia, increased lung sounds, cyanosis, fever, sepsis, death
- Dx: history, clin signs, CBC, culture and cytology of tracheal or lung wash, radiographs
- Ddx: dilated cardiomypathy, heartworm, mycotic pneumonia, pneumocystis pneumonia in immunosuppressed animals, neoplasia, influenza
- Tx: antibiotics, supportive care, oxygen
Abscesses in ferrets
- Staphylococcus spp, Streptococcus spp, Corynebacterium spp, Pasteurella, Actinomyces, hemolytic E. coli, Aeromonas spp
- Of lung, liver, uterus, vulva, skin, mammary glands, oral cavity
- May result from wounds inflicted by biting during fighting, playing, mating, chewing sharp objects
- Clin signs: localized swellings +/- draining tracts - usually SC abscesses are walled off & don’t cause systemic signs; may see dental abscesses d/t canine tooth fracture; stranguria d/t prostatic abscessation - often secondary to hyperadrenocorticism
- Dx: cytology & Gram staining of aspirate
- Ddx: myiasis, granuloma, hematoma, neoplasia
- Tx: prevent exposure to sharp objects, limit exposure of male and female during breeding, antibiotics & establish drainage
Mastitis in ferrets - etiology, transmission
- G(+) cocci like Streptococcus spp, Staphylococcus aureus & coliforms like hemolytic E. coli most frequently associated
- Factors that may be involved: stress of lactation, injury to mammary glands by kits, environmental contamination, virulence of the organism
- Organism may be present in oral cavity of kits
Mastitis in ferrets - clin signs, diagnosis
- Acute form: occurs soon after parturition or after 3rd week of lactation - glands are swollen, firm, red or purple, painful, may become gangrenous
- Chronic form: may occur when kits are 3 weeks old or as sequela to acute form = glands that are firm but NOT painful or discolored
- Dx: history, clin signs, PE findings, isolation of organism
- E. coli often positive for cnf1 = tend to produce extraintestinal disease & are referred to as necrotoxigenic E. coli
Mastitis in ferrets - pathology, treatment
- Glands swollen, overlying skin discolored
- Edema, hemorrhage, coagulative & liquefactive necrosis of glandular tissue & surrounding SC tissue
- Mixed leukocytic infiltrate - primarily PMN leukocytes, large numbers of bacteria, thombosis and necrosis of vessels
- Tx: broad-spectrum antibiotics; recommend oral administration of antibiotics to nursing kits also; surgical resection & debridement may be needed for acute mastitis; kits may spread infection to foster jills!; good hygiene to minimize spread to other jills; euthanisia for chronic mastitis
Canine distemper in ferrets
- Paramyxovirus; genus Morbillivirus (related to measles, rinderpest)
- Several strains, including a ferret adapted strain
- Virus can be inactivated by heat, light, phenol, Roccal, sodium hydroxide, formalin
- Most serious viral infection of ferrets; mortality up to 100%
- Catarrhal Phase: 7-10 days postinfx; anorexia, pyrexia, photosensitivity, serous nasal discharge, erythematus pruritic rash (cell-mediated immunity to infected endothelial cells), hyperkeratosis of footpads (not always seen); secondary bacterial - mucopurulent ocular and nasal discharge, pneumonia
- CNS Phase: ataxia, tremors, paralysis; may or may not be preceded by catarrhal phase
- Death in 12-16 days from ferret strains, up to 35 days from canine strains
Canine distemper in ferrets - transmission, epizootiology
- Virus shed in conjunctival, nasal, oral exudates, urine, feces, sloughed skin
- Ferrets very susceptible to infection via respiratory route
- Viremia detectable 2 days postinfection & persists until ferret mounts a neutralizing antibody response
- Primary site of replication = respiratory and lymphatic systems
- Decrease in lymphocyte subsets at 5-30 days postinfection
- Moves to CNS via infection of vascular endothelial cells and hematogenous spread of virus infected leukocytes from meningeal blood vessels into the subarachnoid space = widespread infection of cells of pia and arachnoid mater of the leptomeninges over large areas of the cerebral hemispheres
Canine distemper in ferrets - clin signs, diagnosis
- Intracytoplasmic & intranuclear inclusion bodies in tracheal, bronchial epithelia; bile duct; transitional epithelium of bladder
- Inclusions = eosinophilic (H&E) inclusions, appear orange using Pollack’s trichrome stain
- Dx: fluorescent antibody test on peripheral blood & conjunctival mononuclear cells; RT-PCR; cytology of conjunctival scrapings
- Ddx: Bordetella bronchiseptica, influenza (does not rapidly progress to mucopurulent ocular and nasal discharge like CD)
Canine distemper in ferrets - treatment, control
- Isolate clinically affected ferrets; euthanasia recommended as no reports of animals surviving acute infection
- Vaccination can prevent infx: MLV of chicken embryo tissue culture origin (CETCO) given IM
- Vaccinate kits every 2-3 weeks from 6 weeks old to 14 weeks, then annually
- Vaccine reactions have been reported following double-dose vaccination (follow schedule above) - vomiting, diarrhea, fever, collapse
- Treat vaccine reaction with diphenhydramine IV or IM or epinephrine SC, IV, IM, intratracheal
- Inactivated vaccines do not deliver consistent effective immunity = NOT recommended
- CD used to experimentally study mobillivirus infection and vaccine strategies in humans
Experimental infection of ferrets with viruses
- Feline panleukopenia, canine parvovirus, canine parainfluenza, mink enteritis virus, respiratory syncytial virus, transmissible mink encephalopathy, pseudorabies
- Natural infection with these viruses has not been reported
Aleutian disease - etiology, transmission
- Aleutian mink disease virus (ADV) = parvovirus in genus Amdoparvovirus, species Carnivore amdoparvovirus 1
- Most common strain = ADV-F
- Mink derived strains more virulent to mink than ferrets; at least 3 strains that are distinct from the mink ADV have been documented in ferrets
- Hypergammaglobulinemia (HGG) = immunomodulation that is disruptive to research
- Transmission: direct or via aerosol of urine, saliva, blood, feces, fomites; vertical transmission established in mink but unproven in ferrets
Aleutian disease - clin signs, diagnosis
- Ferrets infected as adults = persistent infection but rarely disease; chronic progressive weight loss, cachexia, malaise, melena
- May cause ataxia, paralysis, tremors, convulsions
- Lesions typically immune-mediated; elevation of gammaglobulins >20% of the total proteins; in mink there is depression of B & T cell responses
- Dx: HGG and chronic weight loss; IFA or counter-immunoelectrophoresis (CIEP) for antibody to ADV antigen; ELISA & PCR
- Presence of ADV antibody in a ferret is NOT necessarily diagnostic of the disease in an animal (up to 10% of ferrets may be antibody positive without disease)
- DNA of ADV can be detected by in situ hydrixization - can use on paraffin embedded fixed tissues
- Ddx: neurotropic form of canine distemper, chronic wasting diseases like neoplasia, malabsorption, maldigestion, bacterial enteritis
Aleutian disease - treatment, pathology
- Disinfection with formalin, sodium hydroxide, phenolics
- No general treatment, animals should be euthanized
- Mink kits treated with gamma globulin-containing ADV antibody had decrease mortality rates
- Necropsy: may have no lesions; infrequent hepatosplenomegaly & lymphadenopathy
- Histo: periportal lymphocytic infiltrates; bile duct hyperplasia & periportal fibrosis; membranous glomerulonephritis
Influenza in ferrets - etiology
- Orthomyxovirus
- Transmissible from humans to ferrets & ferrets to humans = vaccination of handlers, PPE, don’t work with ferrets if having respiratory illness
- Human influenza viruses A & B pathogenic to ferrets (type B low pathogenicity)
- Ferrets also susceptible to avian, phocine, equine, swine influenza - only swine causes clinical signs
Influenza in ferrets - clin signs, epizootiology
- Remains localized in nasal epithelium but may cause pneumonia
- Clin signs = 48 hr postinfx; anorexia, fever, sneezing, serous nasal discharge, otitis
- Secondary bacterial infection with Streptoccosu spp, Bordetella bronchiseptica
- Transmission: aerosol, direct contact
Influenza in ferrets - diagnosis, treatment, control
- Recovery within 4 days (unlike CDV that progresses to death)
- Dx: clinical signs & recovery within 4 days; hemagglutination inhibition antibody titers on acute and convalescent serum (rarely)
- Tx: amantadine experimentally effective; neuraminidae inhibitors like zanamivir, oseltamivir - these prevent & treat influenza & may be used in combo with amantidin; antibiotics for secondary bacteria
- Ferrets used as influenza model; used in influenza A research to study pathogenesis, Reye’s syndrome, evaluate vaccine trials
Rabies in ferrets
- Rhabdovirus, genus Lyssavirus
- Experimental infection: mean incubation period of 28-33 days, mean morbidity was 4-5 days
- Vaccinate with killed rabies vaccine at 3 mths, 1 year, then annually
- Clin signs: anxiety, lethargy, posterior paresis
- Pathology: Negri bodies may be seen in brain (not always), may be able to isolate virus from salivary glands
- Suspect ferrets that bite or scratch humans = not less than 10 day quarantine for observation
- Recent case report documented recovery and clearance of rabies virus in a ferret - survived for 100 days after onset of clinical signs with continued paraplegia
- Dx: direct IFA of brain tissue
Rotavirus in ferrets - etiology
- Diarrhea in ferret kits - thought to be atypical poorly characterized rotavirus that has not been cultivated in vitro
- Atypical rotaviruses lack the rotavirus common antigen
- Definitive identification of a group C rotavirus in ferrets recently published
Rotavirus in ferrets - epizootiology, transmission, clin signs
- Diarrhea, perineal soiling
- High mortality in young kits, lower mortality if over 10 days of age
- May occur in kits as young as 1-4 days & up to 6 weeks of age
- Secondary bacterial infection may increase severity of diarrhea
Rotavirus in ferrets - pathology, diagnosis, treatment
- Yellow-green liquid of mucous feces in terminal colon
- Subtle small intestinal villous atrophy & epithelial cell vacuolation
- Dx: electron microscopy of centrifuged fecal pellets; CANNOT use commercially available enzyme immunoassays
- Tx: mortality reduced if kits continue nursing - syringe feed milk replacer; supportive care
- Jills develop immunity to rotavirus infection & subsequent litters are protected
Epizootic catarrhal enteritis in ferrets - etiology, transmission
- A novel Alphacoronavirus = ferret enteric coronavirus (FRECV)
- Occurs when young animal introduced to a colony of adults. though susceptible animals can be infected at any age
- Virions shed in feces and saliva; intermittent shedding possible long after resolution of clinical disease
- Transmission: rapid infection by oral route
- High morbidity, low mortality
- Considered enzootic
Epizootic catarrhal enteritis in ferrets - clin signs, diagnosis
- Decreased appetite, weight loss, lethargy, diarrhea - green mucoid, vomiting, dehydration
- If chronic, malabsorption can occur & feces become small, ovoid
- Elevated liver enzymes & nonspecific hematologic abnormalities in some ferrets
- Young ferrets have milder disease than older ferrets
- Dx: intestinal biopsy & histopath with IHC; RT-PCR; electron microscopy; a serologic test exists but should be evaluated in context of clinical signs
Epizootic catarrhal enteritis in ferrets - pathology, treatment
- Enteritis with watery intestinal contents, enlarged mesenteric LNs
- Histo: LYMPHOCYTIC ENTERITIS WITH VILLOUS ATROPHY & necrosis and vacuolzation of enterocyte tips; villous blunting and fusion
- Lesion are in JEJUNUM & ILEUM
- Tx: aggressive oral & systemic fluid therapy; antibiotics for secondary bacteria; metronidazole
- Most detergents and disinfectants will kill environmental coronavirus
Ferret systemic coronavirus - etiology, transmission, clin signs
- Systemic granulomatous disase due to ferret systemic coronavirus (FRSCV)
- Genus Alphacoronavirus - behaves similarly to FIP dry form
- Typically affects animals under 1 year of age
- Transmission: mechanism unknown, but likely ingestion
- Clin signs: lethargy, decreased appetite, diarrhea, vomiting, weight loss; some animals have neuro signs of ataxia, paresis, tremor, head tilt, seizure
Ferret systemic coronavirus - diagnosis, pathology, treatment
- Histo: intralesional coronaviral nucleic acid; IHC using monoclonal antibody (FIPV3-70) will localize nucleic acid
- RT-PCR capable of differentiating FRSCV & FRECV
- Clin signs + hematology strongly suggestive - nonregenerative anemia, hyperglobulinemia, hypoalbuminemia, thrombocytopenia
- Ddx: Aleutian disease - due to FRSCV polyclonal gammopathy
- Radiography & endoscopy for palpated masses
- Necropsy: enlarged mesenteric LNs; multiple tan coalescencing nodules on serosal surfaces & mesenteric vessels
- Histo: lesions most common in liver, kidney, spleen, lung; severe pyogranulomatous inflammation often surrounding vessels that infiltrates and destroys affected parenchyma; brain = pyogranulomatous meningoencephalitis
- Tx: supportive care incl. iron in anemic animals, vitamins, gastroprotectants, immunostimulatory antibiotics like doxycycline
- Most animals die or are euthanized within weeks of diagnosis
Bovine herpesvirus 1 in ferrets
- Infectious bovine rhinotracheitis (IBR)
- Isolated from liver, spleen, lung of clinically normal ferrets
- Raw beef suspected as source of infection
- In experimental infection of ferrets, IBR caused either no respiratory pathology OR acute suppurative pharyngitis
Hepatitis E virus in ferrets
- Isolated from 4 ferrets in the Netherlands
- No overt signs of disease
- Relevance to ferret health or zoonotic risk unknown
Suid herpesvirus 1 in ferrets
- Pseudorabies virus (PRV), Aujeszky’s disease
- Consumption of raw pork by ferrets
- Usually fatal in most species infected
Coccidiosis in ferrets - etiology, clin signs
- 3 species of Isospora and Eimeria reported in ferrets: Isospora laidlawi, Eimeria furonis, Eimeria ictidea
- Transmission: ingestion of sporulated oocysts
- Clin signs: usually subclinical; diarrhea, lethargy, dehydration; rectal prolapse; one case of biliary infestation with E. furonis
- Clin signs more common in young newly acquired ferrets after a stressful event
Coccidiosis in ferrets - diagnosis, treatment
- Dx: fecal float, direct wet mount; infestation of biliary tract resulted in changes on serum chemistry
- Pathology: jejunum & ileum - villous and epithelial thickening; parasitic cysts and microorganisms within epithelium; mild granulomatous inflammation in villar lamina propria
- Ddx: GI foreign body; dietary indiscretion, nutritional, inflammatory, infectious, other systemic diseases - proliferative colitis, salmonellosis, giardiasis, rotavirus, campylobacteriosis, eosinophilic gastroenteritis
- In biliary case: hepatomegaly, enlarged firm bile ducts, thickened gallbladder wall
- Control: good husbandry; cleaning cages with strong ammonium hydroxide solution; heat treatment of surfaces and utensils
- Tx: sulfadimethozine for 6 days; ponazuril (triazine coccidiocidal drug) for 10 days
- As with dogs and cats, the complete elimination of a coccidial infection requires an immunocompetent host
Cryptosporidiosis in ferrets - etiology, transmission, clin signs
- Etiology: Cryptosporidium spp.
- Class Sporozoa, Subclass Cocidia
- Inhabits respiratory and intestinal epithelium of birds, reptiles, mammals. fish
- Transmission: ingestion of sporulated oocysts in contaminated food, water; life cycle similar to other coccidian parasites; autoinfection characteristic of life cycle
- Clin signs: subclinical in both immunocompetent & immunosuppressed ferrets reported; otherwise nonspecific clinical signs with death possible in 48-72 hr
Cyrptosporidiosis in ferrets - diagnosis, pathology, treatment
- Dx: sugar solution centrifugation or fecal sedimentation using formalin-ether or formalin-ethyl acetate; direct fecal smear with methanol or heat fixing & stained with acid-fast - oocysts small compared to other coccidia - spherical to ellipsoidal; acid-fast; oocyst residuum is seen as a refractive dot under phase-contrast
- Pathology: spherical to ovoid 2-5 um diameter organisms associated with brush border of villi; mild eosinophilic infiltrate in lamina propria of small intestine; ILEUM MOST COMMON HEAVILY INFECTED SECTION of small intestine
- Tx: no known definitive treatment; supportive/symptomatic care; infections self-limiting in immunocompetent
- ZOONOTIC
- Drying, freeze-thawing, and steam cleaning inactivate the organism; few effective commercial disinfectants
Sarcoptic mange in ferrets
- Sarcoptes scabiei
- Transmission: direct contact with infected hosts or fomites
- Ferrets have Generalized or Pedal Form
- Generalized: lesions are focal or generalized alopecia with intense pruritis
- Pedal: lesions confined to toes and feet; feet become swollen with scabbing, nails may be deformed or lost
- Dx: skin scraping or removing crusts, breaking them up, & clearing with 10& KOH for microscopic exam
- Ddx: other pruritic external parasites like fleas; demodicois causes mild pruritis and alopecia in ferrets
- Tx: Pedal = trim claws, remove scabs after softening in warm water; ivermectin SC or selamectin or lime sulfur dips; shampoos or soaks to reduce pruritis; antibiotics for secondary bacteria
Demodicosis in ferrets
- Demodex spp.
- Found in normal skin, not considered contagious; predisposing factors incl immunologic or genetic conditions
- Clin signs: alopecia, pruritis, orange discoloration of skin behind ears or on ventral abdomen & accompanying seborrhea
- Dx: deep skin scraping; skin biopsy may be needed in chronic cases with thickened skin
- Pathology: mites with a short, blunted abdomen similar to Demodex criceti; epidermis hypertrophic, mild superficial orthokeratotic hyperkeratosis, mild perivascular & superficial mixed cellular infiltrate
- Ddx: sarcoptic mange, fleas, primary/secondary bacterial dermatitis
- Tx: amitraz dip; imidacloprid-moxidectin; ivemectin orally or topically; selamectin
Ear mites in ferrets
- Otodectes cynotis
- Transmission: direct contact with infested animal; entire life cycle completed in 3 weeks
- Clin signs: usually asymptomatic; head shaking, mild to severe pruritis with inflammation & excoriation; secondary otitis interna with ataxia, circling, torticollis, Horner’s syndrome; brownish-black waxy discharge
- Dx: otoscopic exam, microscope evaluation of ear slides
- Tx: topical treatments more efficacious than injectable; ivermectin; due to anatomic characteristics of ferret ear, instillation of drops into the ear canal is of very limited efficacy; selamectin; imidacloprid-moxidectin; can give medications partially in ear canal & partially at interscapular region
- High doses of ivermectin (0.2 mL of 1% solution) administered to jills at 2-4 weeks gestation resulted in high rates of congenital defects
Fleas in ferrets
- Ctenocephalides species
- Transmission: direct contact with another infested animal or flea-infested environment
- Clin signs: asymptomatic; mild to intense pruritis and alopecia of dorsal thorax and neck
- Dx: clin signs, identification of fleas or flea excrement
- Ddx: sarcoptic mange, demodex
- Tx: concurrent treatment of environment & all animals in household is essential; rotenone or pyrethrin powders or sprays; selamectin topical; imidacloprid topical
Pneumocystis carinii in ferrets
- Fungus
- Inhabits lungs of many different species; recent transmission studies suggest these fungi are highly species specific
- Clin signs: only seen in immunocompromized ferrets (such as induced using high dose steroids)
- Pathology: interstitial pneumonitis with mononuclear cell infiltrates
- Dx: cysts and trophozites are evident with Gomori methanamine-silver nitrate and Giemsa on bronchoalveolar lavage
- Tx: trimethoprim-sulfamethoxazole probably controls but does NOT eliminate infection
Mucormycosis in ferrets
- Ferrets susceptible o secondary fungal infection of outer ear canal with Absidia corymbifera or Malassezia spp.
- These fungi widespread in environment & will cause secondary fungal infection in ears of ferrets infested with Otodectes cynotis
- Dx: impression of ear exudates
- Tx: eradicate underlying mite infestation followed by oral and topical ketoconazole, miconazole and polymyxin B
Dermatomycosis in ferrest
- Microsporum canis & Trichophyton mentagrophytes
- ZOONOTIC
- Control infection with general disinfection and destruction of contaminated beddings
- Clin signs: circumscribed areas of alopecia inflammation that begin as small papules & spread peripherally in a scaly inflamed ring
- Dx: yellow-green fluorescence of M. canis under UV light; skin scrapings digested with 10% KOH
- Tx: griseofulvin causes clinical remission but may not clear infx
Cryptococcosis in ferrets
- Cryptococcus neoformans, Cryptococcus gatti
- Immune suppression might be a contributing factor
- Cryptococcus is found in soil, bird droppings, and trees
- Prognosis is guarded and treatment is usually difficult
- Tx: itraconazole for 10 months resulted in a successful outcome for C. neoformans variety grubii isolated from an enlarged submandibular LN
Other ectoparasites of ferrets
- Hypoderma bovis: granulomatous masses in cervical region
- Cuterebra larvae: subdermal cysts in subcutis of nec
- Flesh fly: infestation reported in commercially reared mink and ferrets housed outdoors
- Ticks: may be found on ferrets housed outdoors
Heartworm in ferrets - etiology, epizootiology, transmission
- Dirofilaria immitis - filarial parasite transmitted by mosquitos
- Microfilaria ingested by mosquitos and, after 2 molts, become infective 3rd stage larvae - infected larvae deposited into skin when mosquitos feed - larvae find way into body and migrate SC to thorax and eventually heart
- Primary reservoir of infection is dogs, but heartworm may be found in a variety of mammals
- All species except wild & domestic canids, domestic felines, ferrets, and California sea lions are considered aberrant hosts
Heartworm in ferrets - clin signs, dx, treatment
- Weakness, lethargy, depression, dyspnea, cyanosis, anorexia, dehydration, cough, pale MMs; moist lung sounds, muffled heart sounds; pleural or abdominal effusion; caval syndrome, mild anemia, biliverdinuria - may be of increased diagnostic value for this condition in ferrets
- Dx: clin signs, radiography/US, microfilaremia - not consistent, testing for heartworm antigen may be more useful
- Pathology: cardiomegaly, pleural and/or abdominal fluid and pulmonary congestion; adult worms in R atrium, R ventricle, pulmonary artery, cranial & caudal vena cava; microfilaria in small & large vessels in lungs
- Ddx: primary cardiac disease - DCM; other systemic or pulmonary diseases
- Tx: Prevent with monthly oral ivermectin or topical selamectin year-round (0.006 mg/kg body weight monthly); treatment with thiacetarsemide (same precautions as dogs - antithromboic therapy, treatment for heart failure, strict cage confinement); ivermectin until clin sins & microfilaremia resolve; melarsomine NOT recommended d/t adverse reactions
Other nematodes in ferrets
-Ferrets are susceptible to infection with: Toxascaris leonina; Toxocara cati; Ancylostoma spp.; Dipylidium caninum; Mesocestoides spp.;
Atriotaenia procyonis; Trichinella spiralis; Filaroides martis; and Spiroptera nasicola
Pregnancy toxemia in ferrets - etiology
- Most common in primiparous jills carrying large litters; an inadvertant fast in late pregnancy is sometimes indicated
- At least 75% of jills carrying more than 8 kits will develop if subjected to 24 hr of food withdrawal
- Any jill with 15 of more kits may develop because abdominal space inadequate for uterus & amount of food required
- Abnormal energy metabolism with hyperlipiemia, hypoglycemia, ketosis, hepatic lipidosis, decreased T4 and T3 levels
- Excessive mobilization of free fatty acids
Pregnancy toxemia in ferrets - clin signs, diagnosis, pathology, treatment
- Anorexia, lethargy, melena, dehydration, easily epilated hair
- Ddx: dystocia, metritis, pyometra, septicemia, renal failure, Helicobacter mustelae-induced gastric ulcer
- Dx: azotemia, hypocalcemia, hypoproteinemia, elevated liver enzymes, anemia
- Pathology: tan or yellow discolored liver, gastric hemorrhage, gravid uterus
- Tx: if jill within a day of delivery, C-section and intensive postop support - force feeding gruel of high quality cat food & ferret chow, IV fluids with glucose, supplemental heat’ perform C-section under isoflurane or sevoflurane b/c metabolism of injectable agents prolonged by hepatic dysfunction
- Agalactia common after C-section - hand feed or cross foster kits
- Develop toxemia before 40 days of gestation = fluids & nutritional support until C-section can be performed
- Prevention: feed highly palatable diet with >20% fat and >35% crude protein, avoid stress & dietary changes
Hyperestrogenism in ferrets - etiology, clin signs
- Ferrets are induced ovulators and may remain in persistent estrus if they are not bred or if estrus is not terminated chemically or by OVH
- Estrogen-indued anemia possible in jills that remain in estrus for more than 1 month
- Hyperestrogenism causes bone marrow hypoplasia of all cell lines in half of ferrets in prolonged estrus
- Clin signs: vulvar enlargement, bilaterally symmetric alopecia of tail and abdomen, weakness, anorexia, depression, lethargy, weight loss, bacterial infection, mucopurulent vaginal discharge
- Initial neutrophilia & thrombocytosis then lymphopenia, thrombocytopenia, neutropenia, anemia
- Anemia begins as normocytic normochromic & progresses to macrocytic hypochromic
- Coagulopathy assoc w/ hepatic dysfunction, thrombocytopenia = bleeding, pallor, melena, petechiation or ecchymosis, subdural hematoma, hematomyelia
Hyperestrogenism in ferrets - pathology, treatment
- Tissue pallor, light tan to pale pink bone marrow, hemorrhage, bronchopneumonia, hyddrometra, pyometra, mucopurulent vaginitis
- Histo: cystic endometrial hypoplasia, hemosiderosis, diminised splenic extramedullary hemtopoiesis, mild to moderate hepatic lipiosis
- Tx: terminate estrus & supportive care with antibiotics, blood transfusion, B vitamins, nutritional support
- Estrus may be terminated by injection of 50-100 IU HCG or 20 ug of GnRH, repeated 1 week later if needed; OVH
- PCV 25% or greater - good prognosis; PCV 15-25% guarded & may need blood transfusion; PCV less than 15% - poor prognosis
- Repeated administration of hCG may result in sensitization and anaphylaxis - incoordination, tremor, vomiting, diarrhea - reverse with diphenhydramine; GnRH is smaller molecule = anaphylaxis less likely, GnRH implant is available
- Estrogen induced anemia can be avoided by OVH, use of vasectomized hovs, or pharmacologic termination of estrus initiated 10 days after estrus onset
Hyperammonemia in ferrets
- Administration of arginine-free diets to young ferrets fasted for 16 hr leads to hyperammonemia and encephalopathy within 2-3 hr
- Exacerbation of signs may be achieved by challenging young ferrets with influenza virus and aspirin - constitutes a model of Reye’s syndrome in children
- Clin signs: lethargy, aggressiveness; then prostration, coma, death
- Presumably occurs because of inability of ferrets to produce adequate amounts of ornithine from non-arginine precursors - detoxificaton of ammonia is therefore compromised
- Ferrets older than 18 mths are unaffected by arginine-free diets
Zinc toxicosis in ferrets
- Ferrets of all ages are susceptible
- Leaching of zinc from steam-sterilize galvanized food and water bowls
- Clin signs: pallor, posterior weakness, lethargy
- Dx: elevated levels of zinc in kidney and liver
- Pathology: kidneys enlarged, pale, soft; livers orange; gastric hemorrhage
- Histo: glomerular collapse, tubular dilation, tubular proteinaceous debris, focal cortical fibrosis, hepatic periacinar infiltration, depresstion of erythroid series
- Avoid galvanized materials
Hypothyroidism in ferrets
- Clin signs: obesity, lethargy, decreased activity, excessive sleeping
- Dx: measure T4 levels using human recombinant TSH
- Tx: oral levothyroxine every 12 hr
Traumatic disorders in ferrets
- Fighting: separate hobs at 12 weeks of age to avoid
- Traumatic elbow luxation: common in ferrets; typically occurs when animal changes directions after getting a leg caught in cage flooring; open reduction should be used because closed reduction rarely successful = tranarticular pin for 4 weeks with leg splinted until after pin removal
Iatrogenic disorders in ferrets
- Hydronephrosis due to ureter ligation & ovarian remnants = both related to OVH surgery
- Ovarian remnants assoc w/ estrus, vulvar enlargement, alopecia
4 major categories of neoplasia in ferrets
- Pancreatic islet cell tumors
- Adrenocortical cell tumors
- Lymphoma
- Skin cancers
Insulinoma in ferrets
- Functional pancreatic islet cell tumors = most common neoplasm in ferrets
- In ferrets as young as 2 years, typically later onset at 4-5 years
- Clin signs: weight loss, vomiting, ataxia; weakness with posterior paresis or collapse, splenomegaly, lymphcytosis; signs often intermittent or episodic
- Hypoglycemia caused by excess production of insulin in neoplastic Beta-cells may cause tremors, disorientation, seizures
- Excessive salivation and pawing at mouth
- Dx: presumptive based on clin signs + hypoglycemia (check after 4 hr fasting period) - fasting glucose below 60 mg/dL considered diagnostic; 60-85 mg/dL suspect; concurrent hyperinsulinemia, but insulin secretion in affected ferrets can be sporadic; histology can provide definitive diagnosis = proliferation of pancreatic Beta-cells; can have local recurrence or mets to LNs, mesentery, spleen, liver
- Ddx: anorexia, starvation, hepatic disease, sepsis, nonpancreatic neoplasia
- Tx: medical management with prednisone +/0 diazoxide along with frequent feeding of high-protein meals; surgery recommended for animals that are healthy enough
Adrenal tumors in ferrets
- Second most common type of neoplasia in ferrets
- Generally diagnosed between 3-6 years of age
- Clin signs: asymptomatic; weight loss, bilateral symmetrical alopecia +/- pruritis
- Clin signs directly related to increase of sex steroids in the blood resulting in estrogen toxicity
- Difference between this condition and typical Cushing presentation is the production in affected ferrets of a significant increased of sex steroids by the zona reticularis and NOT significant levels of cortisol from the zona fasciculata
- Sex steroids that are usually elevated are estradiol, 17-hydroxyprogesterone, testosterone, androstenedione
- Estrus-like vulva swelling in females; prostatic changes and cystitis in males
- Ddx: ovarian remnant
- Dx: palpation reveals cranial abdominal masses, US shows increased adrenal size; serum assay of sex hormones
- Alopecia can be seasonally intermittent
- Adrenal cortical hyperplasia is extremely common in aging ferrets, even those not showing clinical signs
- Tx: medical management: monthly injection of Lupron (leuprolide acetate) = GnRH superagonist & stops production of LH and FSH - resistant to Lupron may develop over time; Deslorelin implants are treatment of choice; GnRH vaccine for prevention; melatonin - directly inhibits GnRH release; Ferretonin (melatonin implant); surgical exploration and removal of enlarged adrenals; ultrasound-guided alcohol injection into affect adrenal
- Frequently a tumor of the right adrenal will invade into the vena cava = partial resection or removal of vena cava needed; collateral vessels will make up for vena cava; survivors need aggressive fluid therapy for 2-3 days post-op
- Histo: well-differentiated cells with a granular or vacuolated cytoplasm; adrenal cell carcinomas are less commonly found than adenomas & are larger, more pleomorphic, more invasive; mets can occur but are rare
Bilateral adrenalectomy in ferrets
- It is possible to remove both adrenal glands at the same time without creating significant hormonal issues
- Animals should be medicated with dexamethasone during postop recover, & oral prednisone for a few weeks after surgery
- Supplementation with glucocorticoids sometimes needed is the gland remaining after unilateral adrenalectomy has been suppressed by the hyperactive one
Lymphoma in ferrets - etiology, clinical signs
- Seen in all ages; an aggressive form is often seen in juvenile ferrets (less than 2 years of age) - mediastinal mass if often found
- Older ferrets (greaters than 2 years old) more likely to develop more indolent form - multicentric or GI lymphoma
- Potential etiologies: a retrovirus distinct to FeLV; chronic immune stimulation d/t ADV or Helicobacter mustelae (seems responsible for a specific type of gastric B-cell lymphoma)
- Clin signs: often chronic, nonspecific signs - weight loss, anorexia, lethargy, splenic or hepatic enlargement, cutaneous involvement; anemia, lymphopenia or lymphocytosis; atypical lymphocytes in circulation; hypercalcemia with T cell lymphoma; dyspnea with mediastinal mass; elevated liver values, azotemia
- Dx: FNA of masses, radiographs or US; IHC of affected tissues to determine cell immunophenotype
IHC for ferret lymphoma
- Anti-CD3 = B cell lymphoma
- Anti-CD79a = T cell lymphoma
Lymphoma in ferrets - pathology, treatment
- Tan colored masses in lymph nodes, spleen, liver, other organs; diffuse involvement may cause enlargement of these organs or thickening of wall of stomach or intestines
- Histo: neoplastic lymphocytes
- Tx: surgery, chemotherapy, radiation; simplest form of chemotherapy is prednisolone/prednisone - will achieve partial or complete, short term remission
- Chemotherapy may be less effective in ferrets receiving chronic immunosuppression; most chemo regimens are modified feline lymphoma protocols
- The more rapidly progressive form seen in younger ferrets should likely be treated more aggressively than the indolent form seen in adults
- Doxorubicin, and to a lesser extent vincristine, can cause severe tissue sloughing if there is extravasation
Skin tumors in ferrets
- Mast cells tumors are most common integumentary tumors in ferrets - occur anywhere on body with associated alopecia, crusty ulceration, pruritis; histo: well differentiated mast cells with metachromatic cytoplasmic granules - toluidine blue stain
- Basal cell tumors: firm plaques or pedunculated nodules that are white or pink; may grow rapidly and ulcerate; most are benign; Ddx: squamous cell carcinoma, apocrine gland adenocarcinoma
- Chordomas: not epithelial cell tumors, but often present as firm masses on tail, may ulcerate overlying skin; arise along axial skeleton from notochord remnants, slow-growing; generally do not reoccur after tail amputation; prognosis guarded for rare cervical region chordomas - mets documented
Placental-umbilical entanglement in ferrets
- Has been assoc w/ fine particle bedding, large litters, short kit-birth intervals
- Jills may neglect to clean placentas, or kits may be born so rapidly there is not adequate time
- Entangled kits may die d/t dehydration, hypothermia, hypoglycemia
- Tx: dissection under a heat lamp or on a heated surface to free kits; cords should be cut as far away from umbilicus as possible
- Parturition should be supervised, if possible, to avoid entanglement
Congenital defects in ferrets
- Neural tube defect
- Gastrochisis
- Cleft palate
- Amelia
- Corneal dermoids
- Cataracts
- Supernumerary incisors
- Cystic or polycystic kidneys
- Cystic genitourinary anomalies assoc w/ prostate, bladder, proximal urethra likely develop secondary to aberrant hormone secretion by adrenocortical tumors
- Newborn ferrets normally born with closed orbital fissure and are prone to developing subpalpebral abscesses
Cardiomyopathy in ferrets
- Common in aging ferrets
- Dilatative form most commonly diagnosed
- Clin signs: lethargy, weight loss, anorexia; hypothermia, tachycardia, cyanosis, jugular distension, respiratory distress
- Dx: heart murmur/muffled sounds; hepato- & splenomegaly; radiographs; ECG
- Tx: supportive care, diuretics, inotropic drugs
- Long term prognosis is guarded to poor
Splenomegaly in ferrets
- Common finding in ferrets
- May be related to another disease (insulinoma, cardiomyopathy, adrenal tumor, lymphoma, splenic sequestration of erythrocytes with anesthesia) or of unknown significant
- Histo: extramedullary hematopoiesis (EMH) - may be incidental or play role in chronic anemia that may respond to splenectomy = syndrome called hypersplenism
Eosinophilic gastroenteritis in ferrets
- Idiopathic disorder with peripheral eosinophilia of 10-35% (but may not be elevated peripherally), hypoalbuminemia, diffuse infiltration of GI tract with eosinophils
- Incidence is variable
- Clin signs: chronic weight loss, anorexia, diarrhea, vomiting
- Eosinophilic granulomas in mesenteric LNs; sometimes lung or liver may be involved
- Splendore-Hoeppli material in inflamed LNs (Giemsa stain) - this is usually associated with helminths, bacteria, fungi, foreign bodies
- Tx: supportive care for enteritis; ivermectin and corticosteroids may be beneficial
Megaesophagus in ferrets
- Clin signs: weight loss, anorexia, difficulty eating, repeated regurgitation
- Cause generally unknown
- Prognosis is poor, despite efforts at supportive care
Disseminated idiopathic myofasciitis in ferrets
- Emerging ferret disease first described in 2003
- Inflammation of muscle and surrounding tissue
- Ferrets under 18 months most commonly affected
- Clin signs: fever, lethargy, depression, paresis, inappetance; lumbosacral or hind limb pain
- Progressive disability leads to euthanasia in most cases
- PE: wasting, muscle atrophy, lymphadenopathy and splenomegaly
- ALT may be elevated but CK is not; hypoproteinemia and hypoglobulinemia sometimes observed
- Dx: muscle biopsy
- Pathology: areas of pallor or white streaks in various muscle groups including esophagus, diaphragmm, both axial and appendicular skeletal muscle
- Histo: muscle fiber strophy, neutrophilic to pyogranulomatous infiltrate within and around muscle fibers of smooth, cardiac, and skeletal muscle; *transmural and circumferential esophageal infiltrate along the length of the organ is characteristic
- Tx: combination of prednisone, cyclophosphamide, chloramphenicol may be successful
Subpleural histiocytosis/Pleural lipidosis/Lipid pneumonia in ferrets
- Gray, yellow, or white small raised lesion on surface of lungs
- Histo: superficial thickening of lung tissue with mononuclear cell infiltration and varying degrees of fibrosis, with or without cholesterol-like clefts
- Etiology unknown; appears to be incidental lesion